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Exposure to traffic-related fine particulate matter 2.5 causes respiratory damage via peroxisome proliferator-activated receptor gamma-regulated inflammation.
Gong, Xiaolei; Zhu, Limin; Liu, Jinlong; Li, Chunxiang; Xu, Zhuoming; Liu, Jinfen; Zhang, Haibo.
Afiliación
  • Gong X; Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Zhu L; Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Liu J; Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Li C; Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Xu Z; Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Liu J; Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Zhang H; Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Environ Toxicol ; 37(9): 2178-2188, 2022 Sep.
Article en En | MEDLINE | ID: mdl-35670047
ABSTRACT
Exposure to particulate matter 2.5 (PM2.5) potentially triggers airway inflammation. Peroxisome proliferator-activated receptor gamma (PPARγ) has been reported to regulate inflammatory responses in diverse cell types. Therefore, this work investigated the mechanisms of PPARγ in regulating traffic-related PM2.5-induced airway inflammation. Using the diffusion flame burner soot generation, traffic-related PM2.5 was generated and adsorbed. BALB/c male mice and human bronchial epithelial cells (16-HBE) were exposed to PM2.5 alone or co-treatment with rosiglitazone (RSG), an agonist of PPARγ. To the end of exposure, bronchoalveolar lavage fluid (BALF), venous blood and arterial blood, trachea, bronchus and lung tissues were collected. The levels of IL-1ß, IL-6, and IL-17 were detected by ELISA, and the cell types in BALF were counted. Hematoxylin-eosin (H&E) assay were used to analyze the pathological conditions of lung, bronchus, and pulmonary artery. Apoptosis was detected by TUNEL, and PPARγ expression in lung and bronchus was detected by immunohistochemical (IHC) staining. Western Blot was used to detect PPARγ, NF-kB, AP-1 and STAT3 expression in lung and bronchus. The viability was detected by MTT method. PM2.5 exposure caused pathological damage to the lung, bronchus and pulmonary artery tissue, which induced apoptosis of bronchial epithelial cells. PM2.5 exposure caused local inflammation of the whole body and airway. PPARγ expression increased after PM2.5 exposure. PM2.5 exposure regulated the downstream signaling pathways to affect the inflammatory response through PPARγ. Exposure to traffic-related PM2.5 caused respiratory damage via PPARγ-regulated inflammation.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Exposición por Inhalación / PPAR gamma / Material Particulado / Contaminación por Tráfico Vehicular / Inflamación / Enfermedades Pulmonares Tipo de estudio: Etiology_studies Límite: Animals / Humans / Male Idioma: En Revista: Environ Toxicol Asunto de la revista: SAUDE AMBIENTAL / TOXICOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Exposición por Inhalación / PPAR gamma / Material Particulado / Contaminación por Tráfico Vehicular / Inflamación / Enfermedades Pulmonares Tipo de estudio: Etiology_studies Límite: Animals / Humans / Male Idioma: En Revista: Environ Toxicol Asunto de la revista: SAUDE AMBIENTAL / TOXICOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: China